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78 Cards in this Set

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Liver Lobule
portal triad (bile duct, hepatic a., portal v.)
portal vein feeds central vein through limiting plate.
Bile flows opposite to blood
zone 1 (portal tract, highly oxygentated)
zone 2 (intermediate)
zone 3 (central vein, poorly oxygenated)
hepatic endothelial cells
line hepatic sinusoids w/ fenestrae
sievelike communication btwen lumen and space of disse
kupffer cells
phagocytes, 1st line of defense against infection and toxic molecules
stellate cells
beneath endothelial cells in space of disse, storage capacity
liver functions
Metabolic - glucose homeostasis (gluconeogenesis, glycogenolysis), free fatty acids converted to energy or converted to TG
Synthetic - albumin, clotting factors, complement, binding proteins
Storage - glycogen, TG, Fe, Cu, lipid soluble vitamins
Catabolic - endogenous and exogenous substances, released ammonia excreted
Excretory - bile
Regeneration
Billirubin
Arises from the degradation of heme (85% erythrocytes)
Travels in blood bound to albumin (free form is toxic, leads to 'Kernicterus' - irreversible brain injury)
Tranfer from blood to bile:
1) uptake - dissociated from Br taken up by hepatocyte
2) binding - bound to glutathione-S-transferase
3) conjugation - in ER, UGT system conjugates to glucuronic acid
4) excretion - diffuses through cytosol to canaliculus (rate-limiting step)
Some conjugated Br hydrolyzed by normal flora to urobilinogen, absorbed, and excreted in urine
Jaundice
Overproduction of Br - hemolytic dz (rise in unconjugated Br)
Decreased Br uptake - congenital (Crigler-Najjar, Gilbert, Dubin-Johnson, Rotor), Neonatal Jaundice (physiologic)
Impaired Canalicular Bile Flow - Intrahepatic (intrinsic liver dz, intrahepatic cholestasis) extrahepatic (obstruction of large bile ducts) --> incr bile --> pruritus
Liver
Dubin-Johnson
Benign, AR dz, chronic conjugated hyperBr w/ deposition of melanin-like pigment in liver. linked to MRP2 absence
Crigler-Najjar
rare, recessive, unconjugated hyperBr, absence of UGT
Gilbert Syndrome
mild, chronic unconjugated hyperBr, UGT promoter mutations, 3-7% of pop, more common in males, often symptomless or stress induced
Rotor Syndrome
familial conjugated hyperBr, similar to Dubin-Johnson w/o liver pigmentation
Crigler-Najjar
rare, recessive, unconjugated hyperBr, absence of UGT
Gilbert Syndrome
mild, chronic unconjugated hyperBr, UGT promoter mutations, 3-7% of pop, more common in males, often symptomless or stress induced
Rotor Syndrome
familial conjugated hyperBr, similar to Dubin-Johnson w/o liver pigmentation
Bile stasis
prominent bile plus in dilated bile canalliculi
Cholestasis
hepatocytes are swollen and bile stained
necrotic hepatocytes secondary to toxic excess of bile
early - contained in central zone
chronic - bile plugs in periphery
clinical presentation - pruritis, xanthomas, malabsorption
Cholestasis
hepatocytes are swollen and bile stained
liver
extrahepatic biliary obstruction
liver is swollen and bile stained (white bile if prolonged), swollen hepatocytes, diffuse bile pigment, reticulated "feathery" appearance
Bile Infarct (bile lake)
extrahepatic biliary obstruction, necrosis and accumulation of extravasated bile. caused by rupture of dilated bile duct
liver
secondary biliary cirrhosis
cirrhosis
end stage of chronic liver dz, destruction of normal liver architecture by fibrous septa encompassing regenerative nodules
micronodular cirrhosis
nodules slightly larger than a lobule (<3mm), thin CT, active stages contain mononuclear infiltrate and proliferated bile ducts, typical of alcoholic cirrhosis
liver
macronodular cirrhosis
associated w/ chronic hepatitis, and/or confluent necrosis, broad CT, alcoholic micronodular cirrhosis --> macronodular after EtOH cessation
Hepatic Failure
Liver cells unable to sustain vital activities of the liver
most common acute due to viral hepatitis or toxic liver injury
viral hep or cirrhosis most common insidious
leads to hyperBr (direct & indirect), hepatic encephalopathy, Coag defects
Hepatic Encephalopathy
Stage 1 - sleep disturbances, irritability
Stage 2 - lethargy, disorientation Stage 3 - somnolence
Stage 4 - coma
Dx: asterixis, extensor toe responses, decerebrate posture
pathogenesis: increased toxicity due to shunting around liver, increased Ammonia levels (help Dx, not necessary), GABA accentuation, false NTs, phenols, mercaptans
Cerebral edema may be present in acute hepatic failure
Coagulation defects
Thrombocytopenia, DIC, hypoalbuminemia, hepatorenal syndrome (hypoperfusion, reversible)
Secondary endocrine manifestations: gynecomastia, spider angiomas, palmar erythema (estrogen)
Hepatic Failure
Liver cells unable to sustain vital activities of the liver
most common acute due to viral hepatitis or toxic liver injury
viral hep or cirrhosis most common insidious
leads to hyperBr (direct & indirect), hepatic encephalopathy, Coag defects
Hepatic Encephalopathy
Stage 1 - sleep disturbances, irritability
Stage 2 - lethargy, disorientation Stage 3 - somnolence
Stage 4 - coma
Dx: asterixis, extensor toe responses, decerebrate posture
pathogenesis: increased toxicity due to shunting around liver, increased Ammonia levels (help Dx, not necessary), GABA accentuation, false NTs, phenols, mercaptans
Cerebral edema may be present in acute hepatic failure
Coagulation defects
Thrombocytopenia, DIC, hypoalbuminemia, hepatorenal syndrome (hypoperfusion, reversible)
Secondary endocrine manifestations: gynecomastia, spider angiomas, palmar erythema (estrogen)
Portal HTN
sustained increase in portal venous pressure results from obstruction of flow somewhere in portal circuit
Intrahepatic - cirrhosis, schistosomiasis
Prehepatic - portal vein thrombosis
Posthepatic - Budd-Chiari (thrombosis of hepatic vein), hepatic venoocclusive dz (BC variant, occlusion of central veins and hepatic vein branches)
Complications: esophageal and anorectal varices, caput medusae, hypersplenism, Gamna-Gandy bodies (focal hemorrhages w/ fibrotic Fe laden nodules in spleen), ascites
Budd-Chiari
thrombosis of hepatic vein
associated w/: polycythemia vera, hypercoag, malignancies, OC, bacterial infections, paroxysmal nocturnal hemoglobinuria, surgical trauma
liver
acute viral hepatitis
swollen hepatocytes, lymphocytic infiltrate, apoptotic liver cells, councilman bodies (eosinophilic), lobular disarray
HAV - fecal/oral, daycares/travel/homosexual males, never chronic, lifelong immunity
HBV - 10% infected -->carriers, vaccine, causes CD8s to attack hepatocytes, acute/fulminant/chronic, incr risk liver ca.
HDV - coinfection or superinfection w/ HBV
HCV - T-cell response to infected hepatocytes, chronic dz, incr risk hepatobiliary carcinoma, EtOH worsens course
liver
Confluent Hepatic Necrosis
severe variant of acute viral hepatitis, death of almost all liver cells. most common in acute HBV
bridging necrosis, submassive necrosis, massive necrosis
liver
massive hepatic necrosis s/p acute viral hepatitis
nearly all hepatocytes dead
liver
mild chronic hepatisis
liver
severe chronic hepatitis
mononuclear inflammatory infiltrate in expanded portal tract, inflammation penetrating limiting plate surrounding groups of hepatocytes at the border of the portal tract.
Chronic hepatitis w/ cirrhosis
Chronic hepatitis w/ cirrhosis
liver
Ground glass hepatocytes
HBV, hepatocytes w/ HBsAg in cytoplasm (left), staining for HBsAg (right)
Autoimmune Hepatitis
severe chronic hepatitis of unknown cause, circulating Ab & high levels of serum Ig.
Type I - most common, antinuclear & anti-smooth muscle Ab, middle aged women, prolonged asymptomatic course (many present w/ cirrhosis)
Type II - children 2-14 y/o, Ab to liver and kidney microsomes
histologically resembles chronic viral hepatitis
tx: corticosteroids & immunosuppressives, liver transplant
liver
alcoholic fatty liver
EtOH --> fatty liver --> acute alcoholic hepatitis --> cirrhosis
steatosis is reversible (everything is going to be okay)
liver
alcoholic hepatitis
acute necrotizing lesion, predominantly in central zone, hyaline inclusions within hepatocytes (Mallory bodies), neutrophilic inflammatory response, perivenular fibrosis, collagen around central vein (central hyaline sclerosis)
--> malaise, anorexia, fever, RUQ pain, jaundice, mild leukocytosis
STOP DRINKING --> most recover
don't --> 70% cirrhosis
liver
central hyaline sclerosis
collagen deposition around central vein in alcoholic hepatitis
liver
alcoholic cirrhosis
15% of alcoholics
hepatocellular necrosis, signs of fatty liver and/or cirrhosis
STOP DRINKING NOW!!!
Nonalcoholic fatty liver dz
similar histology and progression as alcoholic liver dz
linked to obesity, DM2, hyperlipidemia
Nonalcoholic fatty liver dz
similar histology and progression as alcoholic liver dz
linked to obesity, DM2, hyperlipidemia
liver
Primary Biliary Cirrhosis (inflammatory infiltrate in portal tract w/ bile duct damage)
destruction of intrahepatic bile ducts--> cholestasis --> hepatic damage
typically affects middle aged women
Dx: anti-mitochondrial Ab
correlation w/ other autoimmune dzs
Stage I - ductal lesion
Stage II - scarring
Stage III - cirrhosis
Primary Sclerosing Cholangitis (edematous, fibrotic, and inflamed portal tract. Inflammatory debris is present within the lumen of the bile duct.)
Chronic cholestatic liver dz of unknown cause, inflammation/fibrosis narrow and obstructs intra and extrahepatic bile ducts
2/3 of pts have UC
Stage I - periductal inflammation/fibrosis
Stage II - obliterated bile ducts, fibrous septa in parenchyma
Stage III - secondary biliary cirrhosis
liver
hemochromatosis
hereditary - altered gene expression in intestinal iron absorption (no negative feedback), AR
secondary - many causes
Symptoms: Liver (micronodular cirrhosis --> macronodular cirrhosis), Pancreas (DM2, acinar degeneration), Heart (CHF), Endocrine (loss of libido, amenorrhea, impotence), Joints (arthropathy)
Kayser-Fleischer ring
Wilson's Dz
autosomal recessive 1/100 carrier 1/30,000 live birthes
failure to excrete ceruloplasmin (can't excrete Cu)
Liver (mild to severe chronic hepatitis or cirrhosis)
neuro/psych/optho symptoms
transient acute hemolytic episodes
liver
alpha 1 anti-trypsin deficiency (faintly eosinophilic PAS positive droplets)
autosomal recessive, retention of misfolded protein, micro-->macronodular cirrhosis, emphysema
30% of all cases neonatal hyperBr
incr incidence hepatocellular carcinoma
Kayser-Fleischer ring
Wilson's Dz
autosomal recessive 1/100 carrier 1/30,000 live birthes
failure to excrete ceruloplasmin (can't excrete Cu)
Liver (mild to severe chronic hepatitis or cirrhosis)
neuro/psych/optho symptoms
transient acute hemolytic episodes
liver
alpha 1 anti-trypsin deficiency (faintly eosinophilic PAS positive droplets)
autosomal recessive, retention of misfolded protein, micro-->macronodular cirrhosis, emphysema
30% of all cases neonatal hyperBr
incr incidence hepatocellular carcinoma
hepatotoxin
-always produces liver cell necrosis w/ high enough dose
-extent of hepatic injury is dose dependent
-same lesion(s) in different animal species
-liver necrosis is zonal (typically centrilobular)
-brief interval btwn administration and symptoms
liver
toxic centrilobular necrosis
i.e. acetaminophen, CCl4, mushrooms OD, greater activity of drug metabolizing enzymes in central zones --> more necrosis
pts either die of hepatic favor or recover w/o sequelae
liver
microvesicular fatty liver
i.e. Reye's syndrome
accumulation of TG in hepatocytes. in Reye's also may see hepatic failure, encephalopathy
liver
microvesicular fatty liver
i.e. Reye's syndrome
accumulation of TG in hepatocytes. in Reye's also may see hepatic failure, encephalopathy
Budd-Chiari
thrombosis of hepatic vein
associated w/: polycythemia vera, hypercoag, malignancies, OC, bacterial infections, paroxysmal nocturnal hemoglobinuria, surgical trauma
liver
peliosis hepatis
peculiar hepatic lesion, characterized by cystic, blood-filled cavities that are not lined by endothelial cells. Anabolic sex steroids, contraceptive steroids, and the antiestrogen compound tamoxifen sometimes produce this lesion
liver and nut (not the anatomical one)
Nutmeg liver
chronic passive congestion
s/p R sided heart failure
in severe cases may lead to hepatic fibrosis
pyogenic liver abscesses
staph, strep, gram neg enterics
reach liver via portal blood or biliary tract, arterial blood in septic pt.
pylephlebitic abscess
intraabdominal suppuration transmits organisms
cholangitic abscess
biliary obstruction --> ascending cholangitis --> abscess
typically e. coli
pt presents w/ fever, rapid weight loss, RUQ pain, hepatomegaly, jaundice (25%), elevated AP
tx: drainage if single, multiple difficult tx w/ high mortality
liver
amebic abscess
(next slide: most common parasites)
amebiasis, malaria, leishmania, ascariasis, liver flukes (clonorchis sinensis, fasciola hepatica), echinococcosis
liver
clonorchis sinesis
(next slide most common parasites)
amebiasis, malaria, leishmania, ascariasis, liver flukes (clonorchis sinensis, fasciola hepatica), echinococcosis
liver
neonatal hepatitis
prolonged cholestasis --> liver cell injury and inflammation
causes: 50% unknown 30% alpha1AT deficiency, 20% TORCH, 1% etc (i know 101%, shutup)
giant cell transformation
biliary atresia
lack of a lumen in biliary tree
extrahepatic - causes persistent cholestasis, indication for 1/2 of pediatric liver transplants, hepatitis, chromosomal abnormalities, viral infection
intrahepatic - paucity of bile ducts within the liver, neonatal hep, alagille syndrome (AD, congenital dz), idiopathic
liver
hepatic adenoma
OC linkage, decreased w/ new Rx
encapsulated, pale w/ neoplastic hepatocytes w/o lobular architecture
tumors may rupture and bleed into peritoneum (incr risk w/ preg)
link in men w/ anabolic steroids
liver
focal nodular hyperplasia
central scar w/ fibrous septa radiate
division by multiple fibrous septa resembles cirrhosis
tortuous bile ducts, mononuclear inflammatory cells, absence of lobular architecture
liver
focal nodular hyperplasia
central scar w/ fibrous septa radiate
division by multiple fibrous septa resembles cirrhosis
tortuous bile ducts, mononuclear inflammatory cells, absence of lobular architecture
liver
hepatocellular carcinoma
most common malignant tumor in world, uncommon in western industrialized countries
link w/ chronic HBV and HCV, alcoholic cirrhosis, hemochromatosis, alpha1ATD, Aflatoxin B (fungal contaminant in less developed countries)
presents w/ painful enlarging mass in liver, dismal prognosis
liver
Fibrolamellar HCC
uncommon variant of HCC w/ distinctive histology that appears in normal livers of adolescents/young adults
Eosinophilic tumor cells show a lamellar pattern. A fibrous band (curved arrow) traverses the tumor. Bile casts (straight arrows) are seen within neoplastic acini.
liver
cholangiocarcinoma
originates from biliary tree, predominantly in older pts
high incidence in Asia (C. sinensis), link w/ primary sclerosing cholangitis
metastatic carcinoma
liver involved in 1/3 of matastatic cancers
pt presents w/ weight loss, splenomegaly, ascites, portal HTN, jaundice, hepatic failure
tx: surgical resection
liver
acute rejection
distortion of bile ducts by portal inflammatory infiltrate, atypism of bile duct epithelial cells, inflammation of the ductal epithelium
liver
chronic rejection
more than 2 months, damage to interlobular ducts, progresses to small bile ducts and persistent cholestasis "vanishing bile duct syndrome"
liver
cirrhosis
cirrhosis